Throughout this application, various publications are referenced to as footnotes or within parentheses. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. Full bibliographic citations for these references may be found at the end of this application, preceding the claims.
One of the major indications for electronic pacemaker therapy is high degree heart block, such that a normally functioning sinus node impulse cannot propagate to the ventricle. The result is ventricular arrest and/or fibrillation, and death.
Acute myocardial infarction (MI) afflicts millions of people each year inducing significant mortality and, in a large number of survivors, marked reductions in myocyte number and in cardiac pump function. Adult cardiac myocytes divide only rarely, and the usual response to myocyte cell loss is hypertrophy that often progresses to congestive heart failure, a disease with a significant annual mortality. There have been recent reports of the delivery of mesenchymal stem cells (MSCs a multipotent cell population of blood lineage) to the hearts of post-Mi patients resulting in improved mechanical performance1,2. The presumption in these and other animal studies3, is that the MSCs integrate into the cardiac syncytium and then differentiate into new heart cells restoring mechanical function.